Skeletal Muscle Lipid Content Research Articles

Intramyocellular lipid and glycogen content are reduced following resistance exercise in untrained healthy males

Resistance exercise has recently been shown to improve whole-body insulin sensitivity in healthy males. Whether this is accompanied by an exercise-induced decline in skeletal muscle glycogen and/or lipid content remains to be established. In the present study, we determined fibre-type-specific changes in skeletal muscle substrate content following a single resistance exercise session. After an overnight fast, eight untrained healthy lean males participated in a approximately 45 min resistance exercise session. Muscle biopsies were collected before, following cessation of exercise, and after 30 and 120 min of post-exercise recovery. Subjects remained fasted throughout the test. Conventional light and (immuno)fluorescence microscopy were applied to assess fibre-type-specific changes in intramyocellular triacylglycerol (IMTG) and glycogen content. A significant 27+/-7% net decline in IMTG content was observed in the type I muscle fibres (P<0.05), with no net changes in the type IIa and IIx fibres. Muscle glycogen content decreased with 23+/-6, 40+/-7 and 44+/-7% in the type I, IIa and IIx muscle fibres, respectively (P<0.05). Fibre-type-specific changes in intramyocellular lipid and/or glycogen content correlated well with muscle fibre-type oxidative capacity. During post-exercise recovery, type I muscle fibre lipid content returned to pre-exercise levels within 120 min. No changes in muscle glycogen content were observed during recovery. We conclude that intramyocellular lipid and glycogen stores are readily used during resistance exercise and this is likely associated with the reported increase in whole-body insulin sensitivity following resistance exercise.

Relationship between body composition changes and changes in physical function and metabolic risk factors in aging

Accurate measurement of adiposity in obese children is required for characterizing the condition's phenotype, severity, and treatment effects in vivo. Non-invasive and safe, magnetic resonance imaging and spectroscopy provide an important new approach for characterizing key aspects of pediatric obesity. This review focuses on recent advances in non-invasive magnetic resonance imaging and spectroscopy for quantifying total body and regional adiposity, mapping adipose tissue distribution, and evaluating selected metabolic disturbances in children. The aim is to provide an investigator-focused overview of magnetic resonance methods for use in the study of pediatric body composition and metabolism. Whole body axial images can be rapidly acquired on most clinical magnetic resonance imaging scanners. The images can then be semi-automatically segmented into subcutaneous, visceral, and intramuscular adipose tissue. Specific pediatric studies of errors related to slice gap and number are available. The acquisition of scans in healthy and premature infants is now feasible with recent technological advances. Spectroscopic, Dixon, and other approaches can be used to quantify the lipid content of liver, skeletal muscle, and other organs. Protocol selection is based on factors such as subject age and cost. Particular attention should be directed towards identification of landmarks in growth studies. Recent advances promise to reduce the requirement of subjects to remain motionless for relatively long periods. Magnetic resonance imaging and spectroscopy are safe, practical, and widely available methods for phenotyping adiposity in children that open new opportunities for metabolism and nutritional research.

Skeletal Muscle Lipid and Its Association with Insulin Resistance: What Is the Role for Exercise?

Skeletal muscle lipid content has been associated with insulin resistance and type 2 diabetes. However, intramuscular triglycerides can also be a fuel source for healthy muscle during exercise. The balance between storage and use of muscle triglycerides is likely a key to the interaction between dysregulated fat and glucose metabolism by healthy and insulin resistant muscle.

Physical Activity, Intramuscular Fat, and Insulin Resistance

0007 PURPOSE: Intramyocellular lipid (IMCL) has been associated with insulin resistance of obesity, type 2 diabetes (T2DM) and aging. However, younger endurance-trained athletes are markedly insulin sensitive despite having IMCL similar to those with T2DM, suggesting that this association may be modulated by the oxidative capacity of muscle. We examined the hypothesis that exercise training would increase IMCL, the oxidative capacity of skeletal muscle and insulin sensitivity in older previously sedentary subjects. METHODS: 14 women and 7 men (67.3 ± 0.7 years) participated in an exercise training program designed to elicit improvements in cardiorespiratory fitness (VO2max). Before and after training, histochemical studies of vastus lateralis muscle biopsies were performed to quantify changes in IMCL, oxidative capacity of muscle, and muscle fiber type (N = 13). Changes in muscle lipid content were measured in 8 additional subjects using a novel non-invasive MRI method. Insulin resistance was determined by either the hyperinsulinemic glucose clamp method (n = 8) or the Homeostatic Model Assessment of insulin resistance (HOMA IR)(n = 13). RESULTS: IMCL, quantified by Oil Red O staining (n = 13), increased (p<0.05) from 22.9 ± 1.9 to 25.9 ± 2.6 Arbitrary Units (AU). The oxidative capacity of muscle, determined by SDH staining intensity, significantly increased (p<0.05) from 75.2 ± 5.2 to 83.9 ± 3.6 AU. The percentage of type I fibers determined by anti-myosin immunohistochemistry significantly increased (p<0.05) from 35.4 ± 2.1 to 40.1 ± 2.3%. In this group, there was a trend for HOMA IR to improve as a marker of insulin resistance (2.69 ± 0.43 to 2.38 ± 0.34, P = 0.14). In another group of subjects (n = 8), skeletal muscle lipid content of the gastrocnemius increased following training (7.10 ± 5.84 vs. 10.13 ± 6.54 g/dl; p<0.05). In this group, insulin sensitivity determined by the glucose clamp increased from 10.6 ± 2.2 to 11.6 ± 2.1 mg/kgFFM/min (P<0.05). CONCLUSIONS: Increased IMCL, in the context of enhanced capacity for fat oxidation, may actually represent a positive adaptation to chronic exercise. Future studies should examine the mechanisms by which improved oxidative capacity of muscle is linked with diminished insulin resistance.

β3-adrenoceptor agonist prevents alterations of muscle diacylglycerol and adipose tissue phospholipids induced by a cafeteria diet

BackgroundInsulin resistance induced by a high fat diet has been associated with alterations in lipid content and composition in skeletal muscle and adipose tissue. Administration of β3-adrenoceptor (β3-AR) agonists was recently reported to prevent insulin resistance induced by a high fat diet, such as the cafeteria diet. The objective of the present study was to determine whether a selective β3-AR agonist (ZD7114) could prevent alterations of the lipid profile of skeletal muscle and adipose tissue lipids induced by a cafeteria diet.MethodsMale Sprague-Dawley rats fed a cafeteria diet were treated orally with either the β3-AR agonist ZD7114 (1 mg/kg per day) or the vehicle for 60 days. Rats fed a chow diet were used as a reference group. In addition to the determination of body weight and insulin plasma level, lipid content and fatty acid composition in gastronemius and in epididymal adipose tissue were measured by gas-liquid chromatography, at the end of the study.ResultsIn addition to higher body weights and plasma insulin concentrations, rats fed a cafeteria diet had greater triacylglycerol (TAG) and diacylglycerol (DAG) accumulation in skeletal muscle, contrary to animals fed a chow diet. As expected, ZD7114 treatment prevented the excessive weight gain and hyperinsulinemia induced by the cafeteria diet. Furthermore, in ZD7114 treated rats, intramyocellular DAG levels were lower and the proportion of polyunsaturated fatty acids, particularly arachidonic acid, in adipose tissue phospholipids was higher than in animals fed a cafeteria diet.ConclusionsThese results show that activation of the β3-AR was able to prevent lipid alterations in muscle and adipose tissue associated with insulin resistance induced by the cafeteria diet. These changes in intramyocellular DAG levels and adipose tissue PL composition may contribute to the improved insulin sensitivity associated with β3-AR activation.

Nicotinic acid-induced insulin resistance is related to increased circulating fatty acids and fat oxidation but not muscle lipid content

Insulin resistance is associated with increased circulating lipids and skeletal muscle lipid content. Chronic nicotinic acid (NA) treatment reduces insulin sensitivity and provides a model of insulin resistance. We hypothesized that the reduction in insulin sensitivity occurs via elevation of circulating nonesterified fatty acids (NEFAs) and an increase in intramyocellular lipid (IMCL). A total of 15 nondiabetic males (mean age 27.4 ± 1.6 years) were treated with NA (500 mg daily for 1 week, 1 g daily for 1 week). Insulin sensitivity (glucose infusion rate [GIR]) was determined pre- and post-NA by euglycemic-hyperinsulinemic clamp. Substrate oxidation was determined by indirect calorimetry. Skeletal muscle lipid was assessed by estimation of long-chain acyl-CoA (LCACoA) and triglyceride (TG) content and by 1H-magnetic resonance spectroscopy quantification of IMCL (n = 11). NA reduced GIR (P = .03) and nonoxidative glucose disposal (P < .01) and increased fasting NEFAs (P = .01). The decrease in GIR related significantly to the increase in fasting NEFAs (r2 = .30, P = .03). The intrasubject increase in basal and clamp fat oxidation correlated with the decrease in GIR (r2 = .45, P < .01 and r2 = .63, P < .01). There were no significant changes in muscle LCACoA, TG, or IMCL content. Therefore, induction of insulin resistance by NA occurs with increased availability of circulating fatty acids to muscle rather than with increased muscle lipid content.

Relationship between serum leptin concentration and low-density muscle in postmenopausal women.

The accretion of fat within skeletal muscle has been associated with metabolic abnormalities. Leptin increases muscle fatty acid oxidation and triglyceride hydrolysis. Therefore, leptin concentrations may affect muscle fat content. The objective of this study was to determine if serum leptin concentrations were associated with im lipid content, as reflected in the mid-thigh low-density skeletal muscle area (LDMA). In addition, we evaluated whether hormone replacement therapy (HRT) or ethnicity affected this relationship. Our study population consisted of 80 postmenopausal women aged 45-55 yr, (72 Caucasian and 8 African-American). Both HRT users (n = 50) and nonusers (n = 30) were recruited. Total fat mass was estimated using total body dual-energy x-ray absorptiometry. Fat and muscle areas at the mid-thigh were measured using computed tomography scanning. Results showed that, after adjusting for total fat mass, higher-density muscle area, and ethnicity, higher serum leptin concentration was associated with lower LDMA (P < 0.05). African-American women had greater LDMA than Caucasian women, after controlling for leptin concentration (P < 0.05). Use of HRT did not significantly influence LDMA. These results support the hypothesis that leptin decreases skeletal muscle lipid content, promoting lipid oxidation.

An Increase in Peroxisomal Fatty Acid Oxidation Is Not Sufficient to Prevent Tissue Lipid Accumulation in hHTg Rats

We observed earlier that increased skeletal muscle lipid content in the hereditary hypertriglyceridemic (hHTg) rat is accompanied by a decline in plasma leptin. Leptin has recently been shown to enhance peripheral insulin sensitivity by decreasing the tissue triglyceride accumulation, possibly through regulation of fatty acid oxidation and lipogenesis. Thus, to test the hypothesis that insulin resistance and increased skeletal muscle lipid accumulation in hHTg rats are due to a defect in lipid catabolism, we measured mitochondrial and peroxisomal fatty acid oxidation and malonyl-CoA and acetyl-CoA carboxylase-2 content in skeletal muscles of these animals. In addition, we investigated possible molecular mechanisms responsible for the lower leptin levels in hHTg rats by measuring leptin and leptin-receptor (Ob-Ra) mRNA levels. We found the following: (1) in spite of a higher skeletal muscle malonyl-CoA content and an increased sensitivity of carnitine palmitoyltransferase-1 to malonyl-CoA, carnitine palmitoyltransferase-1 activity in muscle of hHTg rats was normal; (2) increased peroxisomal fatty acid oxidation did not seem to be sufficient to prevent the tissue lipid accumulation in these animals; (3) both lower leptin production by white adipose tissue and increased leptin uptake seem to be responsible for lower circulating leptin levels and therefore lower fatty acid catabolism.

Increased efficiency of fatty acid uptake contributes to lipid accumulation in skeletal muscle of high fat-fed insulin-resistant rats.

In humans and animal models, increased lipid content of skeletal muscle is strongly associated with insulin resistance. However, it is unclear whether this accumulation is due to increased uptake or reduced utilization of fatty acids (FAs). We used (3)H-R-bromopalmitate tracer to assess the contribution of tissue-specific changes in FA uptake to the lipid accumulation observed in tissues of insulin-resistant, high fat-fed rats (HFF) compared with control rats (CON) fed a standard diet. To study FA metabolism under different metabolic states, tracer was infused under basal conditions, during hyperinsulinemic-euglycemic clamp (low FA availability) or during the infusion of intralipid and heparin (high FA availability). FA clearance was significantly increased in the red gastrocnemius muscle of HFF under conditions of low (HFF = 10.4 +/- 1.1; CON = 7.4 +/- 0.5 ml x min(-1) x 100 g(-1); P < 0.05), basal (HFF = 8.3 +/- 1.4; CON = 4.5 +/- 0.7 ml x min(-1) x 100 g(-1); P < 0.01), and high (HFF = 7.0 +/- 0.8; CON = 4.3 +/- 0.5 ml x min(-1) x 100 g(-1); P < 0.05) FA levels. This indicates an adaptation by muscle for more efficient uptake of lipid. Associated with the enhanced efficiency of FA uptake, we observed increases in CD36/FA translocase mRNA expression (P < 0.01) and acyl-CoA synthetase activity (P < 0.02) in the same muscle. FA clearance into white adipose tissue was also increased in HFF when circulating FA were elevated, but there was little effect of the high-fat diet on hepatic FA uptake. In conclusion, insulin resistance induced by feeding rats a high-fat diet is associated with tissue-specific adaptations that enhance utilization of increased dietary lipid but could also contribute to the accumulation of intramuscular lipid with a detrimental effect on insulin action.

Skeletal Muscle Lipid Content and Insulin Resistance: Evidence for a Paradox in Endurance-Trained Athletes

Skeletal Muscle Lipid Content and Insulin Resistance: Evidence for a Paradox in Endurance-Trained Athletes

Skeletal muscle lipid content and insulin resistance: evidence for a paradox in endurance-trained athletes.

We examined the hypothesis that an excess accumulation of intramuscular lipid (IMCL) is associated with insulin resistance and that this may be mediated by the oxidative capacity of muscle. Nine sedentary lean (L) and 11 obese (O) subjects, 8 obese subjects with type 2 diabetes mellitus (D), and 9 lean, exercise-trained (T) subjects volunteered for this study. Insulin sensitivity (M) determined during a hyperinsulinemic (40 mU x m(-2)min(-1)) euglycemic clamp was greater (P < 0.01) in L and T, compared with O and D (9.45 +/- 0.59 and 10.26 +/- 0.78 vs. 5.51 +/- 0.61 and 1.15 +/- 0.83 mg x min(-1)kg fat free mass(-1), respectively). IMCL in percutaneous vastus lateralis biopsy specimens by quantitative image analysis of Oil Red O staining was approximately 2-fold higher in D than in L (3.04 +/- 0.39 vs. 1.40 +/- 0.28% area as lipid; P < 0.01). IMCL was also higher in T (2.36 +/- 0.37), compared with L (P < 0.01). The oxidative capacity of muscle determined with succinate dehydrogenase staining of muscle fibers was higher in T, compared with L, O, and D (50.0 +/- 4.4, 36.1 +/- 4.4, 29.7 +/- 3.8, and 33.4 +/- 4.7 optical density units, respectively; P < 0.01). IMCL was negatively associated with M (r = -0.57, P < 0.05) when endurance-trained subjects were excluded from the analysis, and this association was independent of body mass index. However, the relationship between IMCL and M was not significant when trained individuals were included. There was a positive association between the oxidative capacity and M among nondiabetics (r = 0.37, P < 0.05). In summary, skeletal muscle of trained endurance athletes is markedly insulin sensitive and has a high oxidative capacity, despite having an elevated lipid content. In conclusion, the capacity for lipid oxidation may be an important mediator of the association between excess muscle lipid accumulation and insulin resistance.

Independent influences of central fat and skeletal muscle lipids on insulin sensitivity.

Insulin resistance is closely associated with two disparate aspects of lipid storage: the intracellular lipid content of skeletal muscle and the magnitude of central adipose beds. Our aim was to determine their relative contribution to impaired insulin action. Eighteen older (56 to 75 years of age) men were studied before elective knee surgery. Insulin sensitivity (M/Delta I) was determined by hyperinsulinemic-euglycemic clamp. Central abdominal fat (CF) was assessed by DXA. Skeletal muscle was excised at surgery and assayed for content of metabolically active long-chain acyl-CoA esters (LCAC). Significant inverse relationships were observed between LCAC and M/Delta I (R(2) = 0.34, p = 0.01) and between CF and M/Delta I (R(2) = 0.38, p = 0.006), but not between CF and LCAC (R(2) = 0.0005, p = 0.93). In a multiple regression model (R(2) = 0.71, p < 0.0001), both CF (p = 0.0006) and LCAC (p = 0.0009) were independent statistical predictors of M/Delta I. Leptin levels correlated inversely with M/Delta I (R(2) = 0.60, p = 0.0002) and positively with central (R(2) = 0.41, p = 0.006) and total body fat (R(2) = 0.63, p = 0.0001). The mechanisms by which altered lipid metabolism in skeletal muscle influences insulin action may not be related directly to those linking central fat and insulin sensitivity. In particular, it is unlikely that muscle accumulation of lipids directly derived from labile central fat depots is a principal contributor to peripheral insulin resistance. Instead, our results imply that circulating factors, other than nonesterified fatty acids or triglyceride, mediate between central fat depots and skeletal muscle tissue. Leptin was not exclusively associated with central fat, but other factors, secreted specifically from central fat cells, could modulate muscle insulin sensitivity.

Skeletal Muscle Lipid Content and Oxidative Enzyme Activity in Relation to Muscle Fiber Type in Type 2 Diabetes and Obesity

In obesity and type 2 diabetes, skeletal muscle has been observed to have a reduced oxidative enzyme activity, increased glycolytic activity, and increased lipid content. These metabolic characteristics are related to insulin resistance of skeletal muscle and are factors potentially related to muscle fiber type. The current study was undertaken to examine the interactions of muscle fiber type in relation to oxidative enzyme activity, glycolytic enzyme activity, and muscle lipid content in obese and type 2 diabetic subjects compared with lean healthy volunteers. The method of single-fiber analysis was used on vastus lateralis muscle obtained by percutaneous biopsy from 22 lean, 20 obese, and 20 type 2 diabetic subjects (ages 35+/-1, 42+/-2, and 52+/-2 years, respectively), with values for BMI that were similar in obese and diabetic subjects (23.7+/-0.7, 33.2+/-0.8, and 31.8+/-0.8 kg/m2, respectively). Oxidative enzyme activity followed the order of type I > type IIa > type IIb, but within each fiber type, skeletal muscle from obese and type 2 diabetic subjects had lower oxidative enzyme activity than muscle from lean subjects (P < 0.01). Muscle lipid content followed a similar pattern in relation to fiber type, and within each fiber type, muscle from obese and type 2 diabetic subjects had greater lipid content (P < 0.01). In summary, based on single-fiber analysis, skeletal muscle in obese and type 2 diabetic subjects mani-fests disturbances of oxidative enzyme activity and increased lipid content that are independent of the effect of fiber type.

Skeletal muscle attenuation determined by computed tomography is associated with skeletal muscle lipid content.

The purpose of this investigation was to validate that in vivo measurement of skeletal muscle attenuation (MA) with computed tomography (CT) is associated with muscle lipid content. Single-slice CT scans performed on phantoms of varying lipid concentrations revealed good concordance between attenuation and lipid concentration (r(2) = 0.995); increasing the phantom's lipid concentration by 1 g/100 ml decreased its attenuation by approximately 1 Hounsfield unit (HU). The test-retest coefficient of variation for two CT scans performed in six volunteers was 0.51% for the midthigh and 0.85% for the midcalf, indicating that the methodological variability is low. Lean subjects had significantly higher (P < 0.01) MA values (49.2 +/- 2.8 HU) than did obese nondiabetic (39.3 +/- 7.5 HU) and obese Type 2 diabetic (33.9 +/- 4. 1 HU) subjects, whereas obese Type 2 diabetic subjects had lower MA values that were not different from obese nondiabetic subjects. There was also good concordance between MA in midthigh and midcalf (r = 0.60, P < 0.01), psoas (r = 0.65, P < 0.01), and erector spinae (r = 0.77, P < 0.01) in subsets of volunteers. In 45 men and women who ranged from lean to obese (body mass index = 18.5 to 35.9 kg/m(2)), including 10 patients with Type 2 diabetes mellitus, reduced MA was associated with increased muscle fiber lipid content determined with histological oil red O staining (P = -0.43, P < 0. 01). In a subset of these volunteers (n = 19), triglyceride content in percutaneous biopsy specimens from vastus lateralis was also associated with MA (r = -0.58, P = 0.019). We conclude that the attenuation of skeletal muscle in vivo determined by CT is related to its lipid content and that this noninvasive method may provide additional information regarding the association between muscle composition and muscle function.

Lipolysis in skeletal muscle is rapidly regulated by low physiological doses of insulin.

Both patients with Type II (non-insulin-dependent) diabetes mellitus and normoglycaemic, insulin resistant subjects were shown to have an increased lipid content in skeletal muscle, which correlates negatively with insulin sensitivity. Recently, it was shown that during a hyperinsulinaemic euglycaemic clamp interstitial glycerol was reduced not only in adipose tissue but also in skeletal muscle. To assess whether lipolysis of muscular lipids is also regulated by low physiological concentrations of insulin, we used the microdialysis technique in combination with a 3-step hyperinsulinaemic glucose clamp. Nineteen lean, healthy subjects (12 m/7 f) underwent a glucose clamp with various doses of insulin (GC I = 0.1, GC II = 0.25 and GC III = 1.0 mU x kg(-1) x min(-1)). Two double lumen microdialysis catheters each were inserted in the paraumbilical subcutaneous adipose tissue and in skeletal muscle (tibialis anterior) to measure interstitial glycerol concentration (index of lipolysis) and ethanol outflow (index of tissue flow). During the different steps of the glucose clamp, glycerol in adipose tissue was reduced to 81 +/- 7 % (GC I), 55 +/- 8 % (GC II) and 25 +/- 5 % (GC III), respectively, of basal. In contrast, glycerol in skeletal muscle declined to 73 +/- 5 % (GC I) and to 57 +/- 6 % (GC II) but was not further reduced at GC III. Tissue flow was higher in the skeletal muscle and remained unchanged in both compartments throughout the experiment. This study confirms the presence of glycerol release in skeletal muscle. Lipolysis in skeletal muscle and adipose tissue are suppressed similarly by minute and physiological increases in insulin but differently by supraphysiological increases. Inadequate suppression of intramuscular lipolysis resulting in increased availability of non-esterified fatty acids, could represent a potential mechanism involved in the pathogenesis of impaired glucose disposal, i. e. insulin resistance, in muscle. [Diabetologia (1999) 42: 1171-1174]

Lipid content and lipoprotein lipase activity in skeletal muscle of lactating and weaned rats

The aim of the investigation was to study the changes in lipid content and lipoprotein lipase (LPL) activity of skeletal muscle of lactating and weaned rats, in order to gain insight on the role of skeletal muscle in the metabolism of triacylglycerols not used by the mammary gland after weaning. Sprague-Dawley rats fed ad libitum were killed 0, 8, 12, and 24 h after litter separation on the 14th day of lactation. Electron microscopy, as well as determinations of the total fat and phospholipid content were performed on muscles of the right hind limb. Lipoprotein lipase activity was determined in extracts of acetone powder of skeletal muscle, mammary gland, and adipose tissue using dibutyryl fluorescine as substrate. Fat droplets were identified in the muscle interfiber spaces of weaning rats. Muscle total fat and phospholipids were higher in weaned than in lactating rats. After litter separation, lipoprotein lipase activity increased significantly in muscle and in adipose tissue (fourfold), while activity in the mammary gland decreased. The increased muscle lipoprotein lipase activity in the weaned rats seems to be associated with the higher content of fat and with the presence of fat droplets.

The effects of age on substrate depletion and hormonal responses during submaximal exercise in hamsters

Senescent hamsters display a marked reduction in volume of voluntary running. The purpose of this study was to determine whether age differences exist in the pattern of fuel utilization during submaximal exercise, which may account for the reduction in voluntary running. Further, we determined the effects of age on muscle oxidative capacity to assess its relationship to endurance performance in senescent hamsters Depletion of carbohydrate and lipid content of skeletal muscle and liver, and changes in blood concentration of various hormones and substrates during one hour of exercise at 60 percent of VO 2 max served to assess age effects on utilization of metabolic substrates. Exercise produced equivalent depletion of muscle glycogen and similar rise in plasma free fatty acids in young and old hamsters. No exercise effects on skeletal muscle triglyceride concentration or on plasma glycerol, glucagon or catecholamine concentrations were noted. With palmitoyl carnitine as substrate (but not with pyruvate) State 3 respiration of cardiac and skeletal muscle homogenates was lower in old compared to young hamsters. Although old hamsters have a reduced capacity to oxidize lipids in vitro, few age differences in fuel use are evident in vivo during submaximal exercise. Thus, these minor age differences in substrate utilization do not likely account for the substantial reduction in the levels of spontaneous running in senescent hamsters.

Energetics of Sablefish, Anoplopoma fimbria, under Laboratory Conditions

We measured respiration, growth, ingestion, and excretion rates for sablefish, Anoplopoma fimbria, collected off southern California at a depth of 500 m and maintained in the laboratory. We also measured the water, protein, and lipid content of white skeletal muscle in both laboratory-held and field fish. Sablefish fed a large ration (14% of wet body weight) every 7–10 d showed growth rates two to three times higher than known growth rates for field fish. On a reduced ration (4% of wet body weight) sablefish grew at rates similar to field fish, but white muscle composition varied significantly from field fish. Oxygen consumption rates under constant temperature conditions showed a decrease in the weight-specific oxygen consumption rates with increase in body weight, ranging from routine metabolic rates of 195.8 mg O2∙kg−1∙h−1 for a 0.25-kg fish to 60.8 mg O2∙kg−1∙h−1 for a 2.78-kg fish. Based on measurements of respiration and excretion, sablefish were estimated to have 162 d of energy stored in the body lipids and did not show signs of starvation stress with food deprivation up to 6 mo in the laboratory. Energy allocation shows very slow growth rates, low conversion efficiencies, and low metabolic rates as adjustments made to large, infrequent meals.Key words: physiological responses, benthopelagic fish, growth, metabolic rate, respiration, excretion

Uptake and release of free fatty acids and other metabolites in the legs of exercising men.

Uptake and release of free fatty acids and other metabolites in the legs of exercising men.